Cerebral apoplexy, i.e., cerebral infarction, is caused mainly by a thrombus or embolus of the cerebral artery from arteriosclerosis and a cardiac embolism from cardiac diseases. Cerebral infarction caused by cerebrovascular occlusion is classified as cerebral thrombosis and cerebral embolism. Cerebral thrombosis refers to a pathological condition in which arteriosclerosis is caused by hypertension, diabetes, hyperlipidemia, etc., and thereby, an arterial wall becomes thick or hardened. Thus, a blood vessel becomes narrowed causing an inner wall of the blood vessel to be prone to impairment and unevenness, resulting in blood clotting and vascular occlusion. Thus, the blood supply is substantially decreased or blocked so that less oxygen and nutrients are supplied to the brain cells, resulting in cerebral dysfunction. Cerebral embolism refers to a pathological condition in which intracardiac blood flow becomes abnormal due to valvular heart disease, atrial fibrillation, etc., so some blood partially stagnates in the heart and forms clots, which are then detached and occludes a cerebral blood vessel, resulting in a cerebral infarction. Brain oxygen supply interruption over 5˜6 minutes may result in irreversible cerebral change and cerebral tissue necrosis. As a result, the infract area generally experiences anemia, and gradually turns muddy brown. A part of the infract area appears to be congested and another part of the infarct area appears to have scattered petechial hemorrhage. Cerebral oxygen deficiency or blood leakage into a cerebral tissue may cause impairment of a cerebral tissue, cerebral edema, and a change in sensation and adjustment. Serious cerebral edema has a risk for increased intracranial pressure. An intracellular fluid and an extracellular fluid are primarily accumulated in the white matter. A brain with edema has many dents and becomes heavy, and thus pressurizes the ventricular system.
Degenerative cerebral disorders develop mainly by apoptosis of neuronal cells, and includes dementia, Parkinson's disease, stroke, Huntington's disease, Creutzfeldt-Jakob disease, Pick's disease, Parkinson-ALS-dementia complex of Guam, Wilson's disease, and progressive supranuclear palsy. Dementia, which is a representative degenerative cerebral disorder, is a cerebral disorder that shows a comprehensive cognitive disorder and is generally caused by a chronic or progressive cerebral disorder. It results in many higher cortical dysfunctions, such as memory, thinking, understanding, calculation, learning, language and judgment disorders. The most common cause of dementia, Alzheimer's dementia (AD), which is one of degenerative cerebral disorder, accounts for about 50 to 60%, vascular dementia (VaD) accounts for 20 to 30%, and others account for 10 to 30%. Alzheimer's dementia (AD) is a pathological condition in which a toxic substance termed Amyloid β (Aβ) is accumulated in the brain and neuronal cells are gradually killed. Clinically, it has a unique progression of very slow development and very slow worsening. The microscopic observation of brains of dead AD patients finds Aβ-accumulated characteristic senile plaque and neurofibrillary tangle. The second most common cause of dementia is vascular dementia that is caused by occlusion or stenosis of cerebral blood vessels (for example, cerebral infarction). Cerebral imaging tests such as CT or MRI find traces of cerebral blood vessel disorders, such as cerebral infarction, cerebral hemorrhages, etc., for patients with vascular dementia.
Most degenerative cerebral disorders are accompanied with dementia, in particular, a cognitive disorder and a memory disorder (memory loss). Accordingly, a therapeutic agent for degenerative cerebral disorders including dementia needs to delay destruction and aging of brain cells to protect brain cells, and recover a cognitive function. Examples of drugs developed heretofore include antioxidants, such as vitamin E and selegiline to suppress destruction of brain cells due to reactive oxygen species, and acetylcholine esterase-inhibiting drugs, such as Tacrine, Aricept, and Exelon. However, these drugs are reported to have serious side effects and low effectiveness. In addition, even healthy people experience decreased memory or concentration probably due to stress by complicated social activities and deteriorated living-environment such as pollution. In response to such problems, it is expected that a drug capable of improving memory may improve memory in people with decreased memory from a degenerative cerebral disorder, aging, or stress, and may allow patients with mental retardation to reconstruct a new memory circuit.
Aralia elata belonging to Araliaceae is distributed in Korea, Japan, China, etc. Shoots of Aralia elata collected in May and June are popular to Koreans as food. While Aralia cordata whose radix is called ‘Aralia’ grows as a trunk from the ground, Aralia elata grows as a shoot and the shoot is collected. Since Aralia elata is a vegetable collected from the top of the head of a tree, it is also called a tree-head-vegetable or a lip-head-vegetable. Aralia elata is known to have anti-diabetic, anti-inflammatory, analgesic, anti-oxidant, and anti-cancer effects. Aralia elata enhances viability, and is very effective for diabetics without any side effect. A bark of Aralia elata Seemann is referred to as Araliae Elatae Cortex. Aralia elata Seem in oriental medicine, and is known to be effective for neuralgia and hypertension. In addition, in oriental medicine, the Aralia elata Seemann bark is known to be effective for an early stage of the flu, neuralgia, and arthritis, have an ataractic effect to remove anxiety, irritation, depression, and have a unique aroma and a bitter taste for increasing appetite. Aralia elata contains a great amount of protein, fat, sugar, fiber, phosphorous, calcium, iron, vitamins (B1, B2, and C), and saponins to decrease blood sugar and blood lipid, and is thus effective for diabetics, nephropathy, and gastroenteric troubles. Korean Patent Publication No. 2006-0072642 discloses an agent for improving cerebral functions, containing an extract from one or two or more selected from the group consisting of Aralia, tree-head-vegetable, Kalopanacis cortex, Phlomis umbrosa, Acyranthes bidentata Blume, and Clematis chinensis Osbeck, in which an extract from a tree-head-vegetable inhibits β amyloid-induced toxicity on neuronal cells and memory loss caused by Scopolamine interrupting the transfer of acetylcoline. However, the published patent does not disclose a prophylactic or therapeutic effect of Aralia elata on cerebral infarction, cerebral edema, cerebral ischemia, or vascular dementia, and does not teach or suggest a remarkable synergic effect of Aralia elata in combination with other components, such as Chaenomelis Fructus and Glycyrrhizae Radix. 
Chaenomelis Fructus, a fruit of Chaenomeles sinensis Koehne (Rosaceae) is known to have an antioxidant effect, an antiviral effect, etc. In addition, it is reported that Chaenomelis Fructus significantly suppresses β-amyloid induced memory impairment in mice, significantly improves an ischemic condition of a cerebral tissue, and suppresses ischemia-induced cerebral tissue impairment (Myeongsin Kim, et al., Journal of Oriental Neuropsychiatry, Vol. 16(1), 2005). However, its remarkable synergic effect in combination with other components, such as Aralia elata and Glycyrrhizae Radix, is not known.
Regarding Glycyrrhizae Radix (the root of Glycyrrhiza uralensis (Lycophodiaceae)), Pal-mul-chong-myeong-tang  including ginseng, Atractylodes macrocephala Koidzumi, white Poria cocos Wolf, Glycyrrhizae Radix, Angelica gigas, Cnidium officinale, Rehmannia glutinosa Liboschitz, Paeonia japonica, Polygala tenuifolia, and Acorus gramineus is known to be effective for suppressing memory loss and learning ability loss due to ischemia (Oriental Medical Graduate School of the Kyung Hee University, Master thesis, Yeongju-Yoon (February, 2006) “Effects of Pal-mul-chong-myeong-tang on Learning and Memorizing in Topical Prosencephalon Ischemia Animal Model.”). However, effectiveness of Glycyrrhizae Radix alone on memory impairment, cerebral infarction, etc. has never been reported.